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Blood, Vol. 95 No. 11 (June 1), 2000:
pp. 3371-3379
Smad7 selectively interferes with different pathways of activin
signaling and inhibits erythroid leukemia cell differentiation
Koki Kitamura,
Shin-ichi Aota,
Ruriko Sakamoto,
Shun-Ichi Yoshikawa, and
Kenji Okazaki
From the Department of Molecular Biology, Biomolecular Engineering
Research Institute, Osaka, Japan.
Smad family proteins are essential for transforming growth factor
 (TGF-) signal mediation downstream of a heteromeric complex of
the type I and type II receptor serine/threonine kinases. A distant
family member, Smad7, is expressed in most mammalian tissues and cells
and prevents TGF- signaling. In this study, we examined the
physiologic role of Smad7 in mediating the effects of activin, a member
of the TGF- superfamily of peptides that functions in a number of
processes, including blood-cell development. We report here that Smad7
expression is specifically absent in particular hematopoietic cells
that respond to activin by differentiating into the erythroid lineage
and that ectopic production of Smad7 causes mouse erythroid leukemia
(F5-5) cells to become resistant to activin induction of erythroid
differentiation. When coexpressed with type I activin receptor ActR-I
or ActR-IB in concert with type II receptor ActR-II, Smad7 efficiently
reduced an early transcriptional response mediated by ActR-I but had
only a minimal effect on the response mediated by ActR-IB. In the
presence of Smad7, overexpression of an activated form of ActR-IB, but
not of an activated form of ActR-I, induced F5-5 cells to
differentiate. These results suggest that Smad7 selectively interferes
with the ActR-I pathway in activin signal transduction. The
findings also indicate the existence of a novel activity of Smad7 that
inhibits erythroid differentiation by blocking intracellular signaling
of activin.
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